Treating iodine deficiency is perhaps best known for being the cheapest and easiest way to reduce brain damage and cognitive impairment in the world. Salt iodization programs cost only around 5 cents per person per year and are effective in raising the population’s iodine status. Dietary iodine is required as an important component of the thyroid hormones. The most visible sign of iodine deficiency is goiter, an unsightly swelling at the front of the neck, is actually caused by a compensatory mechanism that attempts to correct for low iodine intakes. When intakes are low, generally under 100 µg per day, the thyroid gland is triggered to produce greater levels of thyroid stimulating hormone (TSH). The hormone helps the body to take up more iodine from the circulation and to produce more of the thyroid hormones. When this occurs over a long period of time, the thyroid gland increases in size and becomes clearly visible on the front of the neck. Even in the absence of visible goiter, inadequate iodine intakes cause an increase in TSH.

TSH may have other effects on the body in addition to helping to regulate levels of the thyroid hormones. Pearce outlines various mechanisms by which the thyroid hormones and TSH affect lipid metabolism. For example, although it seems that cholesterol production by the liver is actually decreased when thyroid hormone levels are low, there is also a decrease in LDL-cholesterol receptors on various cell types in the body, which leads to a reduced clearance of cholesterol. The net effect is an increase in LDL cholesterol levels. This leads to situations as described by Vierhapper et al., who found that LDL-cholesterol levels were increased in people with overt hypothyroidism.

Recently, Herter-Aeberli and co-workers looked at whether there were effects of correcting elevated TSH with iodine on cardiovascular disease within a clinical trial. 163 overweight or obese women living in Morocco were randomized to 200 µg iodine supplements or a placebo for 6 months. The scarce data on iodine sufficiency in Morocco indicates that the iodine status of the population is poor, and this study confirms this as the women included had a median urinary iodine concentration of only 42 µg/L, a sign of moderate iodine deficiency.

Assignment to iodine treatment reduced TSH concentrations and increased urinary iodine concentrations. Although levels of the thyroid hormones T3 and T4 decreased modestly in both groups over the course of the study, the concentrations of thyroglobulin, used to produce both thyroid hormones, were decreased by the end of the study only in the treatment group. The reductions in both TSH and thyroglobulin indicates that supplementation was effective in improving the iodine status in the women and the need for compensatory measures to increase iodine uptake. In addition, the supplemented women showed a significant decrease in LDL-cholesterol concentrations and leptin concentrations. There were also non-significant decreases in total cholesterol in the supplemented group. Women who had higher baseline cholesterol levels had greater reductions in cholesterol when supplemented.

Sub-clinical iodine deficiency may further exacerbate elevated blood lipids in the overweight and obese. Improving iodine status in an overweight, iodine deficient population has additional effects on cardiovascular disease risk markers. Specifically, iodine supplementation is helpful in reducing elevated LDL-cholesterol . Given that iodine deficiency and overweight/obesity often coexist, in both low- and high-income countries, increasing iodine intakes to adequate levels may be effective in reducing heart disease in older populations, in addition to removing a preventable cause of cognitive impairment in children.